Pathophysiology Module 6

Front 1

hormone on diurnal or circadian rhythm

Back 1

cortical- glucocorticoid produced in adrenal glands that can be produced under stress. increases gluconeogenesis. increases in morning, decreases at night

Front 2

cyclic pattern

Back 2

insulin. basal insulin oscillates around meals. always a constant level that increases or decreases based on carbohydrate.

calcium secretion in islets of langerhans in pancrease controls this.

Front 3

thyroid gland

Back 3

responds to increasing calcium. as it increases, thyroid hormone releases more calcitonin which modulates it

Front 4

feedback

Back 4

how glands communicate so they know how when to start or stop releasing hormones

Front 5

negative feedback

Back 5

system of self regulation that allows for stability

release of one signal signals the release of another and when it reaches adequate levels it signals to stop releasing

thyroid hormone is controlled through this. hypothalamus senses levels of thyroid hormone, if levels are low, thyrotropin releasing hormone is released to anterior pituitary and stimulates release of thyroid stimulating hormone which binds to tsh receptros on thyroid which signals t3 and t4 (thyroid hormones). fills in receptros on hypothalamus to signal shut off

Front 6

positive feedback

Back 6

increase of oxytocin during ferguson reflex (uterine contractions from pressure during childbirth) (more pressure more oxytocin)

Front 7

free form travel

Back 7

water soluble epinephrine or insulin

more available to interact with receptors.

Front 8

serum bound travel

Back 8

testosterone or thyroid

lipid soluble

Front 9

pituitary gland

Back 9

off of hypothalamus in salaturcica.

secretes growth hormone, thyroid hormone, adrenocorticotropin, prolactin

pituitary ademoma- benign tumors on pituitary, incidental lomas (found while trying to find something else), microadenomas (size is very small), don't secrete excess hormones and are asymptomatic normally, can include heminopsia (loss of visual field), apoplexy (acute hemorrhage and necrosis of tumor which can lead to headaches and visual changes)

if on anterior, can lead to acromegaly (gigantism) (enlarged facial, hands and feet, pronounced brow and skull, and growth in internal organs)

can lead to cushing's syndrome (over excretion of cortisol),

Front 10

pituitary adenoma

Back 10

diagnosed from history and physical, over secretion of hormones from pituitary,

headache, visual changes

Front 11

SIDH

Back 11

syndrome of inappropriate antidiuretic hormone

posterior pituitary gland malfunction

over production of ADH

normally secondary to a malignancy or carcinoma of duodenum, stomach, pancreas.

can be caused from encephalitis, meningitis

can be caused from tuberculosis or trauma

can be caused from SSRI, ibuprofen

pathophys: oversecretion of ADH from pituitary or tumor, water retention and volume overload

more aquaporin 2 inserted than what is needed into tubular lining of nephrons. increases total body water. ECF causes dilution of hyponatremia. sodium levels dip, but from dilution instead of a lack of sodium

s/s: headache, thirsty, fatigue, nasea, cramping, muscles twitching from hyponatremia and possible seizures

lab: serum sodium (lower than normal), serum osmolality (also would be low), analysis of urine (urine osmolality greater than 100 because more solute than water) (hyperosmolic) (still secreting sodium, just not water), urine sodium (should also be high)

treatment: stop what is causing it, fluid restriction, sodium tablets (for hyponatremia), loop diuretic if urine osmolality is 2x greater than serum osmolality,

Front 12

diabetes insipidus

Back 12

insufficient ADH. polyuria (excessive urine), neurogenic diabetes (caused from pituitary tumors, injuries to brain, aneurysms, infections of hypothalamus) (decrease in production of ADH)

Nephrogenic (inadequate response of renal tubules to ADH)(direct damage to renal tubules, pilonephritis) (amyloidosis) (polycystic kidney disease) (lithium) (coltrasine for gout) (loop diuretics, antifungal medication)- can't concentrate urine, Unlike in normal diabetes insipidus, this is not due to low levels of ADH, but by an inability for the kidneys to respond it meaning that water is actively secreted

secrete 8-12 liters per day

s/s: polyuria, nocturia (peeing at night), polydypsia (extreme thirst)

tests: serum lab tests (sodium, hypernatremia), high serum osmolality, urine osmolality (low), gravity of liquid (urine is close to being mostly water)

Front 13

thyroid gland

Back 13

manage metabolism and calcium homeostasis

Front 14

hyperthyroidism

Back 14

excess circulating, thyrotoxicosis, extra t3 and t4

causes: primary or secondary

primary hyperthyroidism is from thyroid itself and secondary is from other reasons such as thyroiditis (inflammation of thyroid) (hashimotis thyroiditis- autoimmune disorder, production of antibodies against thyroid that leads to inflammation), postpartum thyroiditis, infectious thyroiditis (from bacteria or virus), graves disease (most common, autoimmune, thyroid autoantibodies that bind to and activate thyroid stimulating hormones (tsh)- over excretion and overgrowth of thyroid)

s/s bulging of eyes, goiter, hypermetabolic, insomnia, tremor, hair loss, diaphoresis, weight loss, heat intolerance, tacchyrhythmia,

diagnosis: measure tsh and thyroid hormone levels. low tsh suggests hyperthyroidism due to negative feedback process.

nodular disease- nodules form and secrete thyroid hormone (iron deficiency)

Front 15

thyroid storm

Back 15

rare. hyperthyroidism. undiagnosed hyperthyroidism or from stress (infection, trauma).

s/s is similar to hyperthyroidism, high fevers, hypertension, tacchycardia, diaphoresis, nausea, vomiting, diarrhea, tremor, coma, seizures.

diagnosis: clinical suspicion, hormone levels (similar to hyperthyroidism)

treatment: beta antagonist, iodine (wolfe- chicoff effect- large quantities inhibit production of thyroid hormone)

Front 16

hypothyroidism

Back 16

not enough thyroid hormone. iodine deficiency (iodine added to salt to fix this), hashimodos thyroiditis, radioactive iodine from nuclear fall out, amniotorone (used for antiarhythmic), hypothalamic (pituitary disfunction),

s/s cold intolerance, constipation, weight gain, bradycardia, fatigue, depression, dry skin, hypotonia, goiter,

Front 17

reinke's edema

Back 17

edema of vocal cords (cracked or hoarse voice) associated with hypothyroidism

Front 18

queen anne's sign

Back 18

hypothyroidism, thinning of outer third of eyebrows

Front 19

diagnostic for hypothyroidism

Back 19

high levels of tsh, low levels of t3 and t4 (primary hypothyroidism)

secondary hypothyroidism, low levels of tsh, t3, and t4

antibodies, prolactin levels,

Front 20

treatment for hypothyroidism

Back 20

replacement of thyroid hormone

Front 21

mixidema coma

Back 21

over exaggeration of hypothyroidism

severe bradycardia, hypotension, decreased consciousness

Front 22

diabetes

Back 22

not enough insulin produced, or cells don't respond to insulin

type I- failure of pancreas to produce insulin

type II-insulin resistance

gestational diabetes

elevations of blood sugar with illness or after steroids are given and sometimes seen in cystic fibrosis and monogenic diabetes

islets of langerhans in pancreas beta cells produce insulin (peptide hormone- released secondary to stimuli (increase of serum glucose) which binds to cell receptor on cell which leads to glut 4 transporters bringing glucose into cell. insulin is then metabolized)

type 1 is loss of beta cells because of antibodies produced to it.

type II- decreased insulin production and increased resistance.

2-5% of pregnancies result in diabetes (large birth weights, resp. distress in babies, hyper billirubinemia)

increased risk of cardiovascular disease, neuropathies, foot ulcers, retinopathies

Front 23

diabetic ketoacidosis

Back 23

type I diabetes

too little insulin- progression of symptoms leading to acidotic state that requires treatment.

hypovolemic due to polyuria, acidotic, positive ketones in serum, hyperosmolar (lots of glucose in blood), metabolic acidosis,

s/s kussmaul's respirations, fruity breath, changes in mental status,

treatment: reverse cause if from stressor, insulin therapy,

can also be from untreated type II and the only difference is you don't see ketones

Front 24

treatment of diabetes

Back 24

medications, type I is insulin (subcutaneously), type II

need to be educated about diet, exercise, and diabetic ulcers in feet, nail care, blood sugar monitoring

Front 25

cushing's disease

Back 25

high levels of cortisol production

increases gluconeogenesis and incrases production of fat

inhibits interleukin receptor to decrease t and b cells

cortisol is high in morning and then lowers

glucocorticoids can lead to this

glucose intolerance (down regulation of glut4 transporter), increase in glycogen storage (hyperglycemia), large weight gain mostly in face and trunk, buffalo hump, central obesity, muscle wasting, stretch marks from decrease in collagen, hypertension, hersitism (facial hair in abnormal pattern)

diagnosed: measure cortisol levels throughout 24 hours,

treatment: from steroids, we stop the steroids, from adenoma or tumor, we remove it

Front 26

addison's disease

Back 26

occurs because of adrenal insufficiency, causes: adrenal disgenesis (adrenal glands don't form properly),

smith lemiopits syndrome -cholesterol synthesis problems (not able to synthesise it)

autoimmune adrenal dysfunction

s/s fatigue, weight loss, low blood pressure, pigmented skin, patchy areas in skin (melanocyte stimulating hormone and adrenocotropin hormone share the same precursor) (also called vitiligo), crisis: stressor from infection or trauma leads to hypertension, hypoglycemia, nausea, hyponatremia, hypercalemia,

acch test: administer hormone and look for increase in cortisol, if they can't increase it then it's addison's.